Parasitism by the protozoan Perkinsus atlanticus favours the development of opportunistic infections

It has been suggested that opportunistic pathogens could contribute to the mortality of Perkinsus atlanticus-infected clams. Examination of Tapes semidecussatus clams from the northern Mediterranean coast of Spain revealed that while 86 % of the clams heavily infected with P. atlanticus were co-infected by bacteria and/or viruses, neither non-infected nor lightly P. atlanticus-infected specimens had bacterial or viral infections. The bacteria, which had a Gram-negative cell wall, were always located in the apical pole of gill epithelial cells and enclosed within membranous compartments. Bacteria-containing cells were hypertrophied and showed dysplasia with loss of cilia and microvilli. The viruses shared ultrastructural, morphologic and cytopathic characteristics of a polyomavirus. Viral particles with icosahedral symmetry were found in both the cytoplasm and the nucleus of numerous cell types. Virus-infected cells showed severe alterations, including hypertrophy, reduction of the intracellular compartments and extrusion of the nuclear envelope. Moreover, gill epithelial cells showed disorganization and swelling of the apical region, which affected the ciliary structure. Our findings show that P. atlanticus parasitism favours the development of opportunistic infections which have detrimental effects in this clam population

When the venerid clam Tapes decussatus is parasitized by the protozoan Perkinsus sp. it synthesizes a defensive polypeptide that is closely related to p225

Molluscs, like other invertebrates, have primitive defense systems. These are based on chemotaxis, recognition and facultative phagocytosis of foreign elements. Previously, we have described one of these systems: a cellular reaction involving infiltrated granulocytes against Perkinsus sp. parasitizing the Manila clam Tapes semidecussatus, in which the parasites are encapsulated by a defensive host product, the polypeptide p225. The aim of this study is to determine the similarities between the defense mechanisms of 2 venerid clams, T. semidecussatus and T. decussatus, when they are infected by Perkinsus sp. The hemocytes of both species infiltrate the connective tissue, redifferentiate, and ultimately, express and secrete the polypeptide which constitutes the main product of the capsule that surrounds the parasites. The main secretion product of T. decussatus shows a high degree of homology to that of T. semidecussatus, since it has a similar electrophoretic mobility and the polypeptide is recognized by the polyclonal serrum against p225 from T. semidecussatus, as confirmed by Western blotting and immunocytochemistry. In conclusion, we demonstrate the existence of 2 polypeptides that are closely related at the molecular and functional level, and are specific in the defense of some molluscs against infection by these protozoan parasites

Characterization and immunolocalization of a main proteinaceous component of the cell wall of the protozoan parasite Perkinsus atlanticus

Described in the present study is a major component of the cell wall of two of the most pathogenic parasites of molluscs, Perkinsus atlanticus and P. marinus. The component is a high-molecular-weight protein (233-kDa), which we have named PWP-1 (for Perkinsus wall protein-1). Western blots, using a polyclonal serum generated against purified PWP-1 from P. atlanticus, revealed that this protein is expressed by all walled developmental stages of this protozoon. By means of immunogold electron microscopy, labelling for PWP-1 was strong and specifically associated with the cell wall. The label density and distribution pattern was quite different between trophozoites and prezoosporangia. With regard to the structural organization of this protein, PWP-1 is disulphide-linked to other cell wall components and released from the cell wall only following treatment with a sulfhydryl agent. We also report that PWP-1 is a trypsin-resistant protein, both in its native and heat-denatured conformation. In addition, results from the N-terminal microsequence of this protein allow us to define PWP-1 as a novel cell wall protein. Overall, our findings strongly suggest that PWP-1 plays a key role in the organization of the cell wall of these protozoa promoting their survival

Improving accuracy and speeding up Document Image Classification through parallel systems

This paper presents a study showing the benefits of the EfficientNet models compared with heavier Convolutional Neural Networks (CNNs) in the Document Classification task, essential problem in the digitalization process of institutions. We show in the RVL-CDIP dataset that we can improve previous results with a much lighter model and present its transfer learning capabilities on a smaller in-domain dataset such as Tobacco3482. Moreover, we present an ensemble pipeline which is able to boost solely image input by combining image model predictions with the ones generated by BERT model on extracted text by OCR. We also show that the batch size can be effectively increased without hindering its accuracy so that the training process can be sped up by parallelizing throughout multiple GPUs, decreasing the computational time needed. Lastly, we expose the training performance differences between PyTorch and Tensorflow Deep Learning frameworks

Lung CD57+ cell density is increased in very severe COPD

Among all inflammatory cells involved in COPD, those with a cytolytic or elastolytic activity are thought to play a key role in the pathogenesis of the disease. However, there is no data about the infiltration of cells expressing the CD57 marker in small airways and parenchyma of COPD patients. In this study, surgical specimens from 43 subjects undergoing lung resection due to lung cancer (9 non-smokers, 18 smokers without COPD and 16 smokers with moderate COPD) and 16 patients undergoing double lung transplantation for very severe COPD were examined. CD57+ cells, neutrophils, macrophages and mast cells infiltrating bronchioles (epithelium, smooth muscle and connective tissue) and parenchymal interstitium were localized and quantified by immunohistochemical analysis. Compared to the other groups, the small airways of very severe COPD patients showed a significantly higher density of CD57+ cells, mainly infiltrated in the connective tissue (p=0.001), and a significantly higher density of neutrophils located characteristically in the epithelium (p=0.037). Also, the density of neutrophils was significantly higher in parenchyma of very severe COPD patients compared with the rest of the groups (p=0.001). Finally, there were significant correlations between the bronchiolar density of CD57+ cells and the FEV1 values (R=-0.43, p=0.022), as well as between the parenchymal density of neutrophils and macroscopic emphysema degree (R=0.43, p=0.048) in COPD groups. These results show that CD57+ cells may be involved in COPD pathogenesis, especially in the most severe stages of the disease

Influence of particle size on extrapleural talc dissemination after talc slurry pleurodesis

Cases of acute respiratory failure reported after talc pleurodesis have raised concerns about its safety. It has been speculated that this pulmonary inflammatory syndrome is secondary to the extrapleural dissemination of the talc particles. Study objectives: To test the hypothesis that particle size influences extrapleural talc deposition and pleural inflammation after talc slurry pleurodesis. Design: Thirty rabbits underwent pleurodesis as follows: 10 rabbits received 200 mg/kg of the talc used for human pleurodesis, normal talc (NT); 10 rabbits received 200 mg/kg of talc with particles of larger size, large talc (LT); and 10 rabbits received saline solution. Samples from the ipsilateral lung, chest wall, diaphragm, mediastinal pleura, heart, liver, spleen, and right kidney were obtained at 24 h and 7 days and processed for optic and electron microscopy and energydispersive x-ray analysis. Results: Visceral pleural thickening was greater with NT than with LT, but no differences were observed in the macroscopic score of adhesions. There was more talc in the lungs of the rabbits that received NT than in those that received LT. Talc particles were detected in mediastinum (100%) and pericardium (20%), irrespective of the talc used. Three animals, all receiving NT, had talc particles in the liver. Conclusions: Our study shows that while both talcs were equally effective in achieving pleurodesis, the intrapleural injection of NT elicits greater pulmonary and systemic talc particle deposition than LT. Moreover, pleural inflammation was greater with NT than with LT

Significant increase of CD57+ cells in pulmonary lymphoid follicles of COPD patients

Although the presence of pulmonary lymphoid follicles (LFs) has been associated with the progression of chronic obstructive pulmonary disease (COPD), there is no information regarding the pattern of vascularisation, expression of addressins or inflammatory cell densities within these structures in COPD. Histological and immunohistochemical techniques were used to assess the prevalence, structure, localisation, vascularisation and cell proliferation/apoptosis of LFs, as well as the follicular density of B- and T-lymphocytes, macrophages, dendritic cells and CD57+ cells, in lung tissue of nine nonsmokers, 18 smokers without COPD, 16 smokers with moderate COPD and 16 patients with very severe COPD. The density of CD57+ cells within LFs of COPD patients was significantly increased compared to that of nonsmokers and smokers without COPD (p<0.05). Moreover, the percentage of LF profiles with cell apoptosis was also significantly higher in COPD patients (p = 0.03). By contrast, no significant differences among groups were observed in the follicular densities of other inflammatory cells, nor in the distribution of blood and lymphatic vessels within LFs. Since CD57+ cells are important effectors of cytotoxicity and immune regulation, an increase in their follicular density supports the hypothesis of local immune dysfunction in COPD

Correction: Deficient pulmonary IFN-β expression in COPD patients

COPD patients are prone to acute infectious exacerbations that impair their quality of life and hamper prognosis. The purpose of the present study was to investigate the in situ IFN-β response in the lungs of stable COPD and non-COPD patients. Lung samples from 70 subjects (9 control never smokers, 19 control smokers without COPD, 21 patients with moderate COPD and 21 patients with very severe COPD) were studied for the expression of IFN-β, its main transcription factor, IRF-7, and two products of its autocrine function, namely RIG-I and MDA-5, by immunohistochemical techniques and quantitative real-time PCR. IFN-β, IRF-7, RIG-I and MDA-5 were widely detected in most lung cell types. In epithelial tissues and alveolar macrophages, IFN-β and IRF-7 labeling scores were decreased up to 65% and 74%, respectively, for COPD patients, paralleling an analogous reduction (43% and 65%, respectively) in the amount of their lung mRNA. Moreover, this decreased production of IFN-β in COPD patients correlated with a similar decrease in the expression of RIG-I and MDA-5, two essential members of the innate immune system. Our study indicates that most lung cells from stable COPD patients show a constitutive decreased expression of IFN-β, IRF-7, RIG-I and MDA-5, suggesting that this deficiency is the main cause of their acute viral exacerbations

Efectores celulares de la respuesta inflamatoria en la enfermedad pulmonar obstructiva crónica

Approximately 3 million people in the world die every year as a consequence of COPD, a pathological process with a high impact also in Chile. COPD is associated with an abnormal inflammatory response of the lung to noxious particles and gases. This inflammatory pattern causes histopathological changes that lead to a narrowing of small airways lumen and destruction of lung parenchyma, also known as emphysema. Classically, these changes were associated to macrophages and neutrophils, although T CD8+ lymphocytes were latter added to the equation, in order to explain the origin of emphysematous lesions. However, in recent years, multiple evidences have arisen indicating that inflammatory response in COPD is much more complex. These findings point to a key role for mast cells, dendritic cells, T CD4+ cells and B cells. The aim of this article is to review such evidence and present what is known so far about the protagonist cells of the inflammatory response in COPD

Active Fragments from Pro- and Antiapoptotic BCL-2 Proteins Have Distinct Membrane Behavior Reflecting Their Functional Divergence

BACKGROUND: The BCL-2 family of proteins includes pro- and antiapoptotic members acting by controlling the permeabilization of mitochondria. Although the association of these proteins with the outer mitochondrial membrane is crucial for their function, little is known about the characteristics of this interaction. METHODOLOGY/PRINCIPAL FINDINGS: Here, we followed a reductionist approach to clarify to what extent membrane-active regions of homologous BCL-2 family proteins contribute to their functional divergence. Using isolated mitochondria as well as model lipid Langmuir monolayers coupled with Brewster Angle Microscopy, we explored systematically and comparatively the membrane activity and membrane-peptide interactions of fragments derived from the central helical hairpin of BAX, BCL-xL and BID. The results show a connection between the differing abilities of the assayed peptide fragments to contact, insert, destabilize and porate membranes and the activity of their cognate proteins in programmed cell death. CONCLUSION/SIGNIFICANCE: BCL-2 family-derived pore-forming helices thus represent structurally analogous, but functionally dissimilar membrane domains